Differential Expression of Cancer-Related miRNAs in Response to Chemotherapeutics and the Regulatory Axis of miR-595/E2F7 in Colorectal Cancer Cells

MicroRNAs (miRNAs) are critical post-transcriptional regulators of gene expression and play key roles in cancer progression and chemoresistance. In this study, we investigated the expression profiles of selected cancer-associated miRNAs in response to two chemotherapeutic agents, docetaxel and lapatinib, in colorectal cancer cell lines. We also explored the potential regulatory interaction between miR-595 and the oncogene E2F7. Colorectal cancer cells (HT-29 and HCT-116) were treated with the IC₅₀ concentrations of docetaxel and lapatinib. RT-qPCR analysis revealed that docetaxel treatment significantly upregulated miR-718, miR-206, miR-1199, and miR-595 in HT-29 cells. In contrast, only miR-206 was upregulated, while the other genes were downregulated in HCT-116 cells. Lapatinib moderately increased the expression of the selected miRNAs in HT-29 cells but consistently downregulated all four miRNAs in HCT-116 cells. Bioinformatic analysis using TargetScan identified E2F7 as a potential target of miR-595. E2F7 expression was found to be elevated in colorectal cancer and further increased in docetaxel-treated HT-29 cells, suggesting a role in drug resistance. Overexpression of miR-595 resulted in the downregulation of E2F7, supporting a regulatory interaction. These findings suggest that miR-595 negatively regulates E2F7 and may contribute to modulating chemoresistance in colorectal cancer. Targeting the miR-595/E2F7 axis may offer a novel therapeutic strategy to enhance the efficacy of chemotherapy in colorectal cancer treatment.